Interspecific differences in crustacean homologous behavior: Neural mechanisms underlying the reversal of uropod steering movement

Summary Rolling of the body in the same direction induces an asymmetrical steering movement of uropods in the opposite directions in two closely related species of crayfish. InProcambarus clarkii the uropod on the upper side is spread out and closed on the lower side, whereas inCambaroides japonicus the uropod moves in the opposite direction. The stimulus detector, the statocysts, the effector, the uropod musculature, are neither structurally nor functionally significantly different in the two species. The results indicate that the opposite responses could be ascribed to differences in the interneuronal connections within the central nervous system of these two species.     

Neural mechanisms of emesis

Emesis is a reflex, developed to different degrees in different species, that allows an animal to rid itself of ingested toxins or poisons. The reflex can be elicited either by direct neuronal connections from visceral afferent fibers, especially those from the gastrointestinal tract, or from humoral factors. Emesis from humoral factors depends on the integrity of the area postrema; neurons in the area postrema have excitatory receptors for emetic agents. Emesis from gastrointestinal afferents does not depend on the area postrema, but probably the reflex is triggered by projections to some part of the nucleus tractus solitarius. As with a variety of other complex motor functions regulated by the brain stem, it is likely that the sequence of muscle excitation and inhibition is controlled by a central pattern generator located in the nucleus tractus solitarius, and that information from humoral factors via the area postrema and visceral afferents via the vagus nerve converge at this point. This central pattern generator, like those for motor functions such as swallowing, presumably projects to the various motor nuclei, perhaps through interneuronal pathways, to elicit the sequential excitation and inhibition that controls the reflex.     

Neural mechanisms of aggression

Unchecked aggression and violence exact a significant toll on human societies. Aggression is an umbrella term for behaviours that are intended to inflict harm. These behaviours evolved as adaptations to deal with competition, but when expressed out of context, they can have destructive consequences. Uncontrolled aggression has several components, such as impaired recognition of social cues and enhanced impulsivity. Molecular approaches to the study of aggression have revealed biological signals that mediate the components of aggressive behaviour. These signals may provide targets for therapeutic intervention for individuals with extreme aggressive outbursts. This Review summarizes the complex interactions between genes, biological signals, neural circuits and the environment that influence the development and expression of aggressive behaviour.     

Neural mechanisms of imitation

Recent advances in our knowledge of the neural mechanisms of imitation suggest that there is a core circuitry of imitation comprising the superior temporal sulcus and the 'mirror neuron system', which consists of the posterior inferior frontal gyrus and adjacent ventral premotor cortex, as well as the rostral inferior parietal lobule. This core circuitry communicates with other neural systems according to the type of imitation performed. Imitative learning is supported by interaction of the core circuitry of imitation with the dorsolateral prefrontal cortex and perhaps motor preparation areas--namely, the mesial frontal, dorsal premotor and superior parietal areas. By contrast, imitation as a form of social mirroring is supported by interaction of the core circuitry of imitation with the limbic system.     

Monoaminergic mechanisms in affective disorders

The monoamine hypothesis of depression originally proposed that depression is caused by a central deficiency of biogenic amines, and antidepressants were considered to work by correcting this deficiency. In the course of time, many studies have analysed monoamine metabolites in the urine, plasma and cerebrospinal fluid of patients and healthy controls under different conditions to test the hypothesis. These studies have failed to identify a robust metabolic disorder in depressive patients as a group. Certain subgroups of depressed patients have shown deviations in biogenic amine metabolism, the most consistent being reduced levels of the major serotonin and dopamine metabolites in the cerebrospinal fluid. Noradrenaline metabolism is influenced by the activity of the sympathetic nervous system, and thus increases in anxious patients regardless of their clinical diagnosis. On the other hand, development of new antidepressants and advances in receptor techniques, together with modern electrophysiologic and behavioural studies have given increasing support to a receptor supersensitivity hypothesis of depression, based on the evidence that antidepressants lead to subsensitivity or down regulation of beta-adrenoceptors, and adaptive changes may occur also in other receptor systems after two three weeks of antidepressant treatment. There is also growing evidence on the manifold interplay of noradrenergic and serotonergic systems in the mechanism of actions of effective antidepressant treatments, including the new and more selective therapeutic compounds. The rapidly increasing knowledge of the neurotransmitter receptors as well as of the relations between the different regulatory systems may lead to more specific intervention strategies in efforts to correct the biological malfunction in the heterogeneous collection of diseases classified as affective disorders.     

Satellite cells in movement disorders of various etiologies

The ultrastructural analysis of the muscle biopsy samples from patients with different neuro-muscular diseases revealed; both degeneration and regeneration of the muscle fibres. The number of satellite cells was increased due to their division and myonuclear segregation. Activated satellite cells were converted into myoblasts which probably could replace the injured fragments of the muscle fibres or form the myotubes. The process of muscle fibre regeneration is restricted not only by the damage of the muscle itself, but by the dystrophic process affecting satellite cells.     

Neural mechanisms of hyperalgesia.

Hyperalgesia, or enhanced sensitivity to pain, is a symptom often associated with inflammation, nerve injury and various diseases. Although hyperalgesia appears to be mediated by sensitization of peripheral and central pain-signalling neurons, underlying mechanisms of sensitization are not well understood. Recent contributions to our knowledge of the mechanisms underlying hyperalgesia and sensitization are reviewed.     

Neural mechanisms of birdsong memory

The process through which young male songbirds learn the characteristics of the songs of an adult male of their own species has strong similarities with speech acquisition in human infants. Both involve two phases: a period of auditory memorization followed by a period during which the individual develops its own vocalizations. The avian 'song system', a network of brain nuclei, is the probable neural substrate for the second phase of sensorimotor learning. By contrast, the neural representation of song memory acquired in the first phase is localized outside the song system, in different regions of the avian equivalent of the human auditory association cortex.     

Neural mechanisms of feature binding

正An object is usually composed of different features (e.g.,color, orientation, and motion), which are processed by segregated visual pathways and represented by functionally specialized brain areas. However, we perceive an object as a coherent whole, rather than its isolated features. How we integrate those isolated features and achieve a precise perception of objects is a fundamental challenge for the visual     

Neural mechanisms in body fluid homeostasis

Under steady-state conditions, urinary sodium excretion matches dietary sodium intake. Because extracellular fluid osmolality is tightly regulated, the quantity of sodium in the extracellular fluid determines the volume of this compartment. The left atrial volume receptor mechanism is an example of a neural mechanism of volume regulation. The left atrial mechanoreceptor, which functions as a sensor in the low-pressure vascular system, is located in the left atrial wall, which has a well-defined compliance relating intravascular volume to filling pressure. The left atrial mechanoreceptor responds to changes in wall left atrial tension by discharging into afferent vagal fibers. These fibers have suitable central nervous system representation whose related efferent neurohumoral mechanisms regulate thirst, renal excretion of water and sodium, and redistribution of the extracellular fluid volume. Efferent renal sympathetic nerve activity undergoes appropriate changes to facilitate renal sodium excretion during sodium surfeit and to facilitate renal sodium conservation during sodium deficit. By interacting with other important determinants of renal sodium excretion (e.g., renal arterial pressure), changes in efferent renal sympathetic nerve activity can significantly modulate the final renal sodium excretion response with important consequences in pathophysiological states (e.g., hypertension, edema-forming states).     

Neural mechanisms involved in pituitary control

The final common pathway of hypothalamo-hypophyseal regulation is composed of neurosecretory neurons elaborating over 20 different neurotransmitters or neuropeptides. Cell bodies of these neurons are located in four major hypothalamic structures (supraoptic and paraventricular nuclei, the preoptic hypothalamic area, and the arcuate-ventromedial region). Their axons build up the tuberoinfundibular bundle, which innervates the median eminence and the posterior pituitary. In those structures, neurosecretory nerve terminals release their secretion product into a microcirculation across neurovascular junctions. Each of the five adenohypophyseal cell types, as well as secretory cells of the intermediate lobe, express specific receptors for several neurotransmitters, many of which are colocalised in the same neuron. In addition, most pituitary neuropeptide receptors are located on more than one cell type. Consequently, pituitary secretion is controlled by multiple neural signals.

Integration of these signals by the cell is achieved by reciprocal interactions between receptor coupling mechanisms. Those involve protein complexes which activate or inhibit adenylate cyclase, as well as mediation by phospholipases. Depending upon its particular mode of coupling, each transmitter-receptor complex can determine activation of phospholipase A or C, phosphoinositide-induced opening of Ca²⁺ channels, or formation of arachidonic acid, a precursor of prostaglandins and leukotrienes. The present chapter reviews the cellular distribution and the coupling pathways of major neural signals driving pituitary functions, and discusses the functional consequences of reciprocal interactions between adenylate cyclase and phospholipase modulation.     

Neural mechanisms of object recognition

Single-unit recordings from behaving monkeys and human functional magnetic resonance imaging studies have continued to provide a host of experimental data on the properties and mechanisms of object recognition in cortex. Recent advances in object recognition, spanning issues regarding invariance, selectivity, representation and levels of recognition have allowed us to propose a putative model of object recognition in cortex.     

Neural mechanisms of persistent aggression

While aggression is often conceptualized as a highly stereotyped, innate behavior, individuals within a species exhibit a surprising amount of variability in the frequency, intensity, and targets of their aggression. While differences in genetics are a source of some of this variation across individuals (estimates place the heritability of behavior at around 25–30%), a critical driver of variability is previous life experience. A wide variety of social experiences, including sexual, parental, and housing experiences can facilitate “persistent” aggressive states, suggesting that these experiences engage a common set of synaptic and molecular mechanisms that act on dedicated neural circuits for aggression. It has long been known that sex steroid hormones are powerful modulators of behavior, and also, that levels of these hormones are themselves modulated by experience. Several recent studies have started to unravel how experience-dependent hormonal changes during adulthood can create a cascade of molecular, synaptic, and circuit changes that enable behavioral persistence through circuit level remodeling. Here, we propose that sex steroid hormones facilitate persistent aggressive states by changing the relationship between neural activity and an aggression “threshold”.     

Neural mechanisms of classical conditioning in mammals

Evidence supports the view that 'memory traces' are formed in the hippocampus and in the cerebellum in classical conditioning of discrete behavioural responses. In the hippocampus learning results in long-lasting increases in excitability of pyramidal neurons that resemble the phenomenon of long-term potentiation. Although it plays a role in certain aspects of conditioning, the hippocampus is not necessary for learning and memory of the basic conditioned responses. The cerebellum and its associated brain-stem circuitry, on the other hand, does appear to be essential (necessary and sufficient) for learning and memory of the conditioned response. Evidence to date supports the view that mossy fibre convey conditioned stimulus information and that climbing fibres conveys the critical 'reinforcement' information to the cerebellum and that 'memory traces' appear to be formed in cerebellar cortex and interpositus nucleus.     

Neural mechanisms of sound localization in owls

Barn owls localize sound by using the interaural time difference of the horizontal plane and the interaural intensity difference for the vertical plane. The owl's auditory system possesses the two binaural cues in separate pathways in the brainstem. Owls use a process similar to cross-correlation to derive interaural time differences. Convergence of different frequency bands in the inferior colliculus solves the problems of phase-ambiguity which is inherent in cross-correlating periodic signals. The two pathways converge in the external nucleus of the inferior colliculus to give rise to neurons that are selective for combinations of the two cues. These neurons form a map of auditory space. The map projects to the optic tectum to form a bimodal map which, in turn, projects to a motor map for head turning. The visual system calibrates the auditory space map during ontogeny in which acoustic variables change. In addition to this tectal pathway, the forebrain can also control the sound-localizing behaviour.     

Patients review: drug-induced movement disorders

Objective of this paper is to review drug-induced movement disorders (D-IMD) treated patients on Department of Neurology in University Hospital Osijek. We reviewed patients treated during 10 years period (from 1992 to 2002). Analysed group consisted of 14 patients. Reasons for hospitalisation were swallowing problems in 6 patients, neuroleptic malignant syndrome (NMS) in 3 patients, stroke in 2 patients, bolus choking in 2 patients, and speech disturbance in 1 patient. Working diagnosis for most of our patients was neurological disease, yet only later D-IMD diagnosis was established excluding primary neurological disease, or as associated disease to basic neurological disorder. Nine patients have diagnosed as Parkinson syndrome, 3 patients as NMS, and 4 as orolingual dyskinesia, either autonomously, or in combination with Parkinson syndrome. D-IMD was most frequently caused by neuroleptics. Thus the small number of patients hospitalised regarding this syndrome on Department of Neurology.     

Thalamic stimulation for control of movement disorders

Chronic recurrent thalamic stimulation has been effective in alleviating a variety of movement disorders. In contrast to thalamic lesions, it is preferred for the treatment of intractable motor disorders in low-risk elderly patients and patients with diffuse brain lesions secondary to trauma. Abnormal diencephalic electrical discharges have been observed and thought to be associated, in some way, with either generating or sustaining the movement abnormalities. The beneficial effects are ascribed to an electrophysiologic functional ablation of the discharging systems. This interpretation is based on the observation that the diencephalic discharges are attenuated by the applied stimulation and that the beneficial effects are reversible even after several months of applied therapeutic stimulation.